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Abstract Background and Hypothesis Deficit schizophrenia (DS) represents a distinct entity characterized by primary and enduring negative symptoms, yet the neurobiological differences between DS and non-DS (NDS) remain undetermined. Using a gradient-based approach, we hypothesize that DS and NDS will exhibit convergent and divergent brain functional hierarchy patterns, each with a specific underlying neurotransmitter architecture. Study Design Resting-state functional magnetic resonance imaging images were acquired from 44 treatment-naive DS, 55 treatment-naive NDS, and 60 matched healthy controls (HCs). Gradient metrics were calculated using the BrainSpace toolbox. The spatial correlation between gradient abnormalities in DS or NDS and density maps of 10 neurotransmitters derived by the JuSpace toolbox was analyzed to link the neuroimaging to underlying neurotransmitter information. Study Results Both DS and NDS exhibited compressed gradient patterns compared to HC, suggesting reduced network differentiation, with more severe disorganization in DS. The ventral attention network was associated with depression symptoms in DS, whereas the visual network was related to total, general, and paranoid symptom scores in NDS. Moreover, spatial correlation of neurotransmitter analysis revealed that the gradient alterations of DS were primarily related to the serotonergic system while those of NDS were predominantly associated with the dopamine system. Conclusions The study suggests that independent from the potential effects of antipsychotic medication, DS and NDS are characterized by different neuropathology in brain hierarchy patterns, potentially linked to neurochemical metabolic distinction. Our findings support the hypothesis that DS is a distinct subtype versus NDS from neurodevelopmental perspective.

Schizophrenia patients show increased disabilities and lower quality of life (DisQoL). Nevertheless, there are no data on whether the activation of the interleukin (IL)-6, IL-23, T helper (Th)-17 axis, and lower magnesium and calcium levels impact DisQoL scores. This study recruited 90 patients with schizophrenia (including 40 with deficit schizophrenia) and 40 healthy controls and assessed the World Health Association QoL instrument-Abbreviated version and Sheehan Disability scale, Brief Assessment of Cognition in Schizophrenia (BACS), IL-6, IL-23, IL-17, IL-21, IL-22, tumor necrosis factor (TNF)-α, magnesium and calcium. Regression analyses showed that a large part of the first factor extracted from the physical, psychological, social and environmental HR-QoL and interference with school/work, social life, and home responsibilities was predicted by a generalized cognitive deterioration (G-CoDe) index (a latent vector extracted from BACs scores), and the first vector extracted from various symptom domains (“symptomatome”), whereas the biomarkers had no effects. Partial Least Squares analysis showed that the IL6IL23Th17 axis and magnesium/calcium had highly significant total (indirect + direct) effects on HR-QoL/disabilities, which were mediated by G-CoDe and the symptomatome (a first factor extracted from negative and positive symptoms). The IL6IL23Th17 axis explained 63.1% of the variance in the behavioral-cognitive-psycho-social (BCPS) worsening index a single latent trait extracted from G-CoDe, symptomatome, HR-QoL and disability data. In summary, the BCPS worsening index is partly caused by the neuroimmunotoxic effects of the IL6IL23Th17 axis in subjects with lowered antioxidant defenses (magnesium and calcium), thereby probably damaging the neuronal circuits that may underpin deficit schizophrenia.

This study compared cognitive domains between deficit schizophrenia (DS) and non-deficit schizophrenia (NDS) patients and healthy controls (HC), analyzing relationships between psychopathological dimensions and cognitive domains. A total of 29 DS patients, 45 NDS patients, and 39 HC subjects participated. Cognitive domains were measured using the Measurement and Treatment Research to Improve Cognition in Schizophrenia Battery. Psychopathological symptoms were evaluated with the Positive and Negative Syndrome Scale. Clinical groups performed poorer than HC groups in regards to speed of processing, attention/vigilance, working memory, verbal and visual learning and memory, reasoning and problem solving, and social cognition. DS patients scored poorer than NDS patients in terms of all cognitive domains and the overall score, except for reasoning and problem solving. Positive, negative, disorganization, and resistance symptoms were related to cognitive functions only in NDS patients. Our findings suggest that the MCCB battery is sensitive to detecting cognitive dysfunctions in both deficit and non-deficit schizophrenia.

The superior longitudinal fasciculus (SLF) is a white matter bundle that connects the frontal areas with the parietal areas. As part of the visuospatial attentional network, it may be involved in the development of schizophrenia. Deficit syndrome (DS) is characterized by primary and enduring negative symptoms. The present study assessed SLF integrity in DS and nondeficit schizophrenia (NDS) patients and examined possible relationships between it and psychopathology. Twenty-six DS patients, 42 NDS patients, and 36 healthy controls (HC) underwent psychiatric evaluation and diffusion tensor imaging (DTI). After post-processing, fractional anisotropy (FA) values within the SLF were analyzed. Psychopathology was assessed with the Positive and Negative Syndrome Scale, Brief Negative Symptom Scale, and Self-evaluation of Negative Symptoms. The PANSS proxy for the deficit syndrome was used to diagnose DS. NDS patients had lower FA values than HC. DS patients had greater negative symptoms than NDS patients. After differentiating clinical groups and HC, we found no significant correlations between DTI measures and psychopathological dimensions. These results suggest that changes in SLF integrity are related to schizophrenia, and frontoparietal dysconnection plays a role in its etiopathogenesis. We confirmed that DS patients have greater negative psychopathology than NDS patients. These results are preliminary; further studies are needed.

This study: (a) compared executive functions between deficit (DS) and non-deficit schizophrenia (NDS) patients and healthy controls (HC), controlling premorbid IQ and level of education; (b) compared executive functions in DS and NDS patients, controlling premorbid IQ and psychopathological symptoms; and (c) estimated relationships between clinical factors, psychopathological symptoms, and executive functions using structural equation modelling. Participants were 29 DS patients, 44 NDS patients, and 39 HC. Executive functions were measured with the Mazes Subtest, Spatial Span Subtest, Letter Number Span Test, Color Trail Test, and Berg Card Sorting Test. Psychopathological symptoms were evaluated with the Positive and Negative Syndrome Scale, Brief Negative Symptom Scale, and Self-evaluation of Negative Symptoms. Compared to HC, both clinical groups performed poorer on cognitive flexibility, DS patients on verbal working memory, and NDS patients on planning. DS and NDS patients did not differ in executive functions, except planning, after controlling premorbid IQ and negative psychopathological symptoms. In DS patients, exacerbation had an effect on verbal working memory and cognitive planning; in NDS patients, positive symptoms had an effect on cognitive flexibility. Both DS and NDS patients presented deficits, affecting the former to a greater extent. Nonetheless, clinical variables appeared to significantly affect these deficits.

BackgroundNegative symptoms are the core of schizophrenia, but whether antipsychotics are efficacious for their treatment is unclear. Moreover, there is debate whether patients in relevant trials should have predominant negative symptoms or whether prominent negative symptoms are also acceptable.MethodsWe systematically reviewed randomised, blinded antipsychotic drug trials in patients with schizophrenia and either predominant or prominent negative symptoms (last search Dec 12, 2017). Separate pairwise meta-analyses were conducted in these two populations. The primary outcome was negative symptoms. Depressive, symptoms, positive symptoms, and extrapyramidal side-effects were analysed as causes of secondary negative symptoms.FindingsWe included 21 randomized-controlled trials with 3451 participants which revealed the following significant differences in the primary outcome: in patients with predominant negative symptoms amisulpride was superior to placebo (N = 4; n = 590, SMD 0.47, CI 0.23, 0.71), olanzapine was superior to haloperidol in a small trial (n = 35) and cariprazine outperformed risperidone (N = 1, n = 456, SMD − 0.29, CI − 0.48, − 0.11). In patients with prominent negative symptoms, olanzapine and quetiapine were superior to risperidone in single trials. Overall, studies in prominent negative symptoms were potentially more confounded by improvements of secondary negative symptoms.InterpretationAmisulpride is the only antipsychotic that outperformed placebo in the treatment of predominant negative symptoms, but there was a parallel reduction of depression. Cariprazine was better than risperidone in a large trial that was well-controlled for secondary negative symptoms, but the trial was sponsored by its manufacturer. Future trials should apply scientifically developed definitions such as the deficit syndrome and the persistent negative symptoms concept.

Background Heterogeneity in the etiology, pathophysiology, and clinical features of schizophrenia challenges clinicians and researchers. A helpful approach could be stratifying patients according to the presence or absence of clinical features of the deficit syndrome (DS). DS is characterized by enduring and primary negative symptoms, a clinically less heterogeneous subtype of the illness, and patients with features of DS are thought to present abnormal brain network characteristics, however, this idea has received limited attention. We investigated functional brain network topology in patients displaying deficit features and those who do not. Design We applied graph theory analytics to resting-state functional magnetic resonance imaging data of 61 antipsychotic medication-naïve first episode psychosis patients, 18 DS and 43 non-deficit schizophrenia (NDS), and 72 healthy controls (HC). We quantified small-worldness, global and nodal efficiency measures, shortest path length, nodal local efficiency, and synchronization and contrasted them among the 3 groups. Results DS presented decreased network integration and segregation compared to HC and NDS. DS showed lower global efficiency, longer global path lengths, and lower global local efficiency. Nodal efficiency was lower and the shortest path length was longer in DS in default mode, ventral attention, dorsal attention, frontoparietal, limbic, somatomotor, and visual networks compared to HC. Compared to NDS, DS showed lower efficiency and longer shortest path length in default mode, limbic, somatomotor, and visual networks. Conclusions Our data supports increasing evidence, based on topological perturbations of the functional connectome, that deficit syndrome may be a distinct form of the illness.

The neurobiological underpinnings of avolition in schizophrenia remain unclear. Most brain imaging research has focused on reward prediction deficit and on ventral striatum dysfunction, but findings are not consistent. In the light of accumulating evidence that both ventral striatum and dorsal caudate play a key role in motivation, we investigated ventral striatum and dorsal caudate activation during processing of reward or loss in patients with schizophrenia. We used functional magnetic resonance imaging to study brain activation during a Monetary Incentive Delay task in patients with schizophrenia, treated with second-generation antipsychotics only, and in healthy controls (HC). We also assessed the relationships of ventral striatum and dorsal caudate activation with measures of hedonic experience and motivation. The whole patient group had lower motivation but comparable hedonic experience and striatal activation than HC. Patients with high avolition scores showed lower dorsal caudate activation than both HC and patients with low avolition scores. A lower dorsal caudate activation was also observed in patients with deficit schizophrenia compared to HC and patients with non-deficit schizophrenia. Dorsal caudate activity during reward anticipation was significantly associated with avolition, but not with anhedonia in the patient group. These findings suggest that avolition in schizophrenia is linked to dorsal caudate hypoactivation.

Abstract Deficit schizophrenia (DS) is a homogeneous subtype of schizophrenia characterized by primary and enduring negative symptoms. However, the underlying neuroanatomical substrate of DS remains poorly understood. Here, we collected high-resolution structural magnetic resonance images of 115 participants, including 33 DS patients, 41 nondeficit schizophrenia (NDS) patients, and 41 healthy controls (HCs), and calculated the cortical thickness and surface area for statistical comparisons among the 3 groups. Relative to the control group, both the DS and NDS groups exhibited convergent cortical thinning in the bilateral inferior frontal gyri and the left superior temporal gyrus. The cortical thinning in the right inferior frontal cortex in the patient group was significantly positively correlated with declines of cognitive flexibility and visuospatial memory. Importantly, compared to the NDS group, the DS group exhibited a more widespread cortical thinning pattern, with the most significant differences in the left temporo-parietal junction area. For the surface area measurement, no significant group differences were observed. Collectively, these results highlight the convergent and divergent cortical thinning patterns between patients with DS and NDS, which provide critical insights into the neuroanatomical substrate of DS and improve our understanding of the biological mechanism that contributes to the negative symptoms and cognitive impairments in DS.

Background The considerable clinical heterogeneity of schizophrenia poses significant challenges for elucidating its neurobiology. The concept of deficit schizophrenia (DS) is a valuable framework for addressing the heterogeneity of schizophrenia. Growing evidence suggests notable differences between deficit (DS) and nondeficit (NDS) schizophrenia, indicating that DS could represent a separate disease entity. Methods We aimed to use FreeSurfer to identify specific changes in cortical thickness among NDS patients and healthy controls (HCs) in a Chinese sample. Furthermore, we examined the potential relationships between changes in cerebral cortical thickness and negative symptoms and attention deficits in DS patients. A total of 142 subjects (48 HCs, 50 NDSs, and 44 DSs) underwent MRI scans and completed the assessment of psychopathological severity and cognitive performance. Results Compared with HCs, DS and NDS patients presented common cortical thinning in the right insula, whereas cortical thinning in the left supramarginal cortex was more prominent in DS patients. We also found that thinning of the temporal and insular cortex was correlated with negative symptoms and impaired attention in DS patients. Conclusions Cortical thinning in specific brain regions in DS patients was found to be correlated with specific clinical and cognitive symptoms.